Monkey claudin 14,CLDN14 ELISA kit
- Known as:
- Monkey claudin 14,CLDN14 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e09c0969
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Monkey claudin 14 CLDN14 ELISA kit
Related genes to: Monkey claudin 14,CLDN14 ELISA kit
- Gene:
- CLDN14 NIH gene
- Name:
- claudin 14
- Previous symbol:
- DFNB29
- Synonyms:
- -
- Chromosome:
- 21q22.13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-26
- Date modifiied:
- 2016-10-05
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- Claudin-14 (CLDN14) is a key component of tight junctions (TJs) critical for maintaining paracellular barrier function. Variants of CLDN14 have been linked to Vein of Galen malformations (VOGMs), a rare cerebrovascular disorder; however, the molecular mechanisms underlying their pathogenicity remain unknown. Here, we investigate the mechanistic effects of two VOGM-associated mutations, A113P and V143M, using reinforcement-learning driven enhanced sampling molecular dynamics simulations combined with DiffNets-based deep learning and independent trajectory-wide structural analyses. Our analysis reveals that A113P induces broader structural disruption of CLDN14, perturbing paracellular sealing, pore symmetry, and inter-protomer communication, whereas V143M induces structural rearrangements centred around TM3 and the TM3-ECL2 region. In both cases, mutation-specific alterations are observed in structural stability and interfacial organization across oligomeric assemblies. Notably, these effects are qualitatively consistent across different modelled architectures, despite variability in local responses. In the absence of experimentally resolved structures, the structural perturbations reported here provide a mechanistic understanding of how VOGM-associated variants may influence CLDN14 structure and dynamics. - Source: PubMed
Publication date: 2026/08/19
Rubina Jamal SehrishXu ManmingAlyemni SalehFan BaojianDuy Phan QZhao ShujuanHale Andrew TKahle Kristopher TMoin Syed TariqueHaider Shozeb - Claudin-14 (CLDN14) is a tight junction protein that contributes to the development of chemoresistant phenotypes in human colorectal cancer (CRC) cells. CLDN14 may represent a potential therapeutic target for CRC. In this study, we identified velpatasvir (VEL), a clinically approved hepatitis C virus nonstructural protein 5 A (NS5A) inhibitor, as a potent suppressor of CLDN14 protein expression using in silico screening and Western blot analysis. CLDN14 expression was not decreased by other NS5A inhibitors, including ledipasvir, pibrentasvir, and daclatasvir. Quartz crystal microbalance analysis revealed that VEL directly binds to recombinant CLDN14 protein with a dissociation constant of 1.8 ± 0.2 μM. VEL treatment did not affect CLDN14 mRNA levels, suggesting that CLDN14 expression is regulated at a post-transcriptional level. Pharmacological inhibition of clathrin-mediated endocytosis and lysosomal degradation significantly reversed the VEL-induced reduction in CLDN14 protein levels, suggesting the involvement of endocytosis-lysosomal degradation pathway. Functionally, VEL increased paracellular permeability to mineral ions and enhanced the transepithelial flux of aqueous fluorescent tracers. In DLD-1 spheroids, VEL attenuated intracellular oxidative stress and reduced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), a central regulator of redox homeostasis. Consequently, VEL promoted the intracellular accumulation of doxorubicin and significantly potentiated its cytotoxic effects. Moreover, VEL enhanced the antitumor efficacy of other chemotherapeutic agents, including oxaliplatin and SN-38, the active metabolite of irinotecan. These findings suggest that VEL enhances anticancer drug sensitivity in CRC cells through lysosome-dependent downregulation of CLDN14 protein and suppression of Nrf2-dependent oxidative stress responses. - Source: PubMed
Publication date: 2026/07/25
Ando TomokaMizukami YukoTosaki ShiemiHashimoto ShotaroIshikawa YoshinobuYoshino YutaMorimoto KazushiShinoda TakehiroShirouzu MikakoEndo SatoshiMatsunaga ToshiyukiMatsuhashi NobuhisaIkari Akira - Claudin-14 (CLDN14), a tight junction protein, contributes to cell proliferation and chemoresistance in human colorectal cancer (CRC)-derived DLD-1 cells. However, small molecules targeting CLDN14 remain unexplored. Here, we identified mupirocin (MUP), a clinically approved topical antibiotic, as a modulator of CLDN14 protein expression. Quartz crystal microbalance analysis revealed interaction between MUP and recombinant CLDN14 protein with a dissociation constant (Kd) of 2.59 ± 0.54 μM. MUP did not alter CLDN14 mRNA levels but reduced CLDN14 protein stability. Pharmacological inhibition of clathrin-mediated endocytosis and lysosomal degradation significantly reversed the MUP-induced reduction of CLDN14 protein. These results suggest MUP accelerates endocytosis-lysosomal degradation of CLDN14 protein. Other antibiotics failed to decrease CLDN14 expression. Functionally, MUP increased paracellular permeability to mineral ions and enhanced the transepithelial flux of doxorubicin (DXR), an anthracycline anticancer drug, and lucifer yellow, an aqueous small compound. In DLD-1 spheroids, MUP reduced intracellular oxidative stress and nuclear factor erythroid 2-related factor 2 (Nrf2) expression. Consequently, MUP promoted intracellular accumulation of DXR and significantly potentiated its cytotoxic effects in spheroids. Moreover, MUP enhanced the antitumor efficacy of other chemotherapeutic agent oxaliplatin. Sulforaphane, an Nrf2 activator, attenuated the MUP-induced enhancement of anticancer efficacy. These findings suggest that MUP enhances anticancer drug sensitivity in CRC through lysosome-dependent downregulation of CLDN14 protein and suppression of oxidative stress signaling. - Source: PubMed
Publication date: 2026/07/06
Mizukami YukoAndo TomokaTosaki ShiemiIshikawa YoshinobuShinoda TakehiroShirouzu MikakoYoshino YutaMorimoto KazushiEndo SatoshiMatsunaga ToshiyukiMatsuhashi NobuhisaIkari Akira - Ampullary cancer is a rare malignancy, histologically divided into intestinal and pancreatobiliary subtypes based on histomorphological and immunophenotypic features as they arise from different epithelial origins and exhibit distinct biological behavior, treatment responses, and clinical outcomes. However, current histomorphological and immunohistochemical classification often remains ambiguous, complicating accurate subtype assignment to guide therapeutic approaches. In this retrospective study of 125 ampullary carcinoma cases, we performed immunohistochemical profiling using a panel of markers including CDX2, CK20, mucins (MUC1, MUC2, MUC5AC), and claudins (CLDN1-4, CLDN7, CLDN18) to refine subtype classification and identify prognostic biomarkers. Hierarchical clustering based on marker expression H-scores revealed two molecular subtypes corresponding to intestinal and pancreatobiliary differentiation. While CDX2 and CK20 are routinely used in combination for diagnosis, other markers, particularly CLDN3, CLDN7, and MUC5AC, demonstrated superior diagnostic and prognostic performance to CDX2. CK20, by contrast, remained a robust marker of intestinal differentiation and favorable outcome. Pancreatobiliary-type tumors exhibited elevated MUC1, MUC5AC, and CLDN18 expression, and were associated with advanced stage, invasive features, and significantly worse survival. Multivariate analysis showed high MUC5AC and apical MUC1 expression to be associated with adverse outcomes, whereas CLDN1, CLDN3 and CLDN4 expression were linked to improved survival. Membranous CLDN18 expression was more common in pancreatobiliary-type ampullary cancer, making it a potential therapeutic target. These findings underscore the diagnostic and prognostic value of multiplex immunohistochemical profiling. We propose retaining CK20 but replacing CDX2 with a more informative marker, namely CLDN3, to enhance classification and therapeutic stratification. - Source: PubMed
Publication date: 2026/07/06
Pein Robert JIllyés IldikóKenessey IstvánPesti AdriánLotz GáborKiss AndrásBorka Katalin - The calcium-sensing receptor (CASR) is a principal regulator of calcium balance. In the kidney, it directly modulates calcium reabsorption in the thick ascending limb (TAL). This review focuses on the CASR in TAL, its role in regulating renal calcium transport and hence systemic calcium homeostasis. - Source: PubMed
Publication date: 2026/06/03
Bogdanovic MilosDimke Henrik